Older news items (pre-2010) brought over from the old website

High protein diet shrinks brain in Alzheimer’s mice

A study using genetically engineered mice has tested the effects of four diets for their effects on Alzheimer’s pathology: a regular diet, a high fat/low carbohydrate custom diet, a high protein/low carb version, or a high carbohydrate/low fat option. Unexpectedly, mice fed the high protein/low carbohydrate diet had brains 5% lighter that all the others, and regions of their hippocampus were less developed. Mice on the high fat diet had higher levels of amyloid-beta protein, although no effect on plaque burden was detected.

Franciosi, S., Gama Sosa, M., English, D., Oler, E., Oung, T., Janssen, W., et al. (2009). Novel cerebrovascular pathology in mice fed a high cholesterol diet. Molecular Neurodegeneration, 4(1), 42. doi: 10.1186/1750-1326-4-42. Full text available at http://www.molecularneurodegeneration.com/content/4/1/40

http://www.eurekalert.org/pub_releases/2009-10/bc-arf101909.php

Infections may lead to faster memory loss in Alzheimer's disease

A 6-month study involving 222 people with Alzheimer's disease (average age 83) has found that people who had infections or even bumps and bruises from a fall were more likely to have high blood levels of tumor necrosis factor-α, a protein involved in the inflammatory process, and were also more likely to experience memory loss or cognitive decline than people who did not have infections and who had low levels of the protein. Nearly half the participants experienced an infection or injury that led to inflammation during the study, and they experienced memory loss that was at twice the rate of those who did not have infections or injuries. Those with high levels of the protein in their blood at the beginning of the study had memory loss at four times the rate of those with low levels of the protein at the start of the study, and those with high levels who also experienced acute infections during the study had memory loss at 10 times the rate of those who started with low levels and had no infections over the six-month period.

Holmes, C. et al. 2009. Systemic inflammation and disease progression in Alzheimer disease. Neurology, 73, 768-774.

http://www.eurekalert.org/pub_releases/2009-09/aaon-iml090109.php

Poor sleep linked to later development of Alzheimer's

A mouse study has found that amyloid-beta significantly increases during periods of sleep deprivation. The discovery follows observation that peptide levels in both mice and humans increase significantly during the day and drop at night. When mice were only allowed to sleep four hours a day for 21 days, they had higher amyloid-beta plaque build-up in their brain than similar-aged mice with regular sleeping habits. The circadian fluctuation was found to reflect the activity of orexin, a hormone that regulates wakefulness. The findings suggest insomnia, late-night habits, and irregular sleep schedules during mid-life may be linked to the later development of Alzheimer's disease.

Kang, J-E. et al. 2009. Amyloid- Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle. Science, Published Online September 24

http://www.the-scientist.com/blog/display/55996/ 
Alzheimers linked to lack of Zzzzs

Greater dementia risk in former N.F.L. players

A study commissioned by the National Football League reports that Alzheimer’s disease or similar memory-related diseases appear to have been diagnosed in the league’s former players vastly more often than in the national population: five times the national average among those 50 and older (6.1%)and 19 times for those aged 30 through 49. The findings are consistent with several recent studies regarding N.F.L. players and the effects of their occupational head injuries. The study involved a phone survey of 1,063 retired players (from an original random list of 1,625), who were asked questions derived from the standard National Health Interview Survey. Some health issues were reported at higher than the population rate (sleep apnea and elevated cholesterol — both risk factors for cognitive problems).

http://www.nytimes.com/2009/09/30/sports/football/30dementia.html

Oxygen treatment hastens memory loss in Alzheimer's mice

A study using genetically engineered mice has found that young adult Alzheimer's mice exposed to 100% oxygen during several 3-hour sessions demonstrated substantial memory loss, while those exposed to normal air had no measurable memory loss, and neither did normal mice without any genetic predisposition for Alzheimer's disease. The results suggest that people genetically predisposed to Alzheimer's disease or with excessive amounts of beta amyloid in their brains are at increased risk of developing the disease earlier if they receive high concentrations of oxygen, for example during or after surgery. The findings may help explain why some elderly patients develop memory loss after major surgery.

Arendash, G.W. et al. 2009. Oxygen treatment triggers cognitive impairment in Alzheimer's transgenic mice. NeuroReport, 20 (12), 1087-1092.

http://www.eurekalert.org/pub_releases/2009-08/uosf-oth081109.php

Delirium rapidly accelerates memory decline in Alzheimer's patients

A new analysis of data spanning 15 years and involving 408 Alzheimer’s patients, has revealed that among those 72 patients who developed delirium at some point, the average decline on cognitive tests was 2.5 points per year before the episode of delirium, and 4.9 points per year after. Across groups, the rate of decline was about three times faster in those who had delirium compared to those who did not. Delirium often develops in elderly patients following a medical disturbance, surgery or infection, but it is preventable in up to 40% of cases.

Fong, T.G. et al. 2009. Delirium accelerates cognitive decline in Alzheimer disease. Neurology, 72, 1570-1575.

http://www.eurekalert.org/pub_releases/2009-05/bidm-dra043009.php

Connection between heart disorder and Alzheimer's

A very large study, involving over 37,000 patients, has found that those with atrial fibrillation, regardless of age, were 44% more likely to develop dementia, and those younger than 70 were 130% more likely to develop Alzheimer's. Previous studies have shown a connection between atrial fibrillation and vascular dementia. Atrial fibrillation is the most common heart rhythm problem, and has a strong genetic link. It is also a risk factor for stroke.

The findings were presented Friday, May 15, at "Heart Rhythm 2009," the annual scientific sessions of the Heart Rhythm Society in Boston.

http://www.eurekalert.org/pub_releases/2009-05/imc-smf051309.php

Inflammatory response to infection and injury may worsen dementia

Systemic inflammation – inflammation in the body as a whole – is known to have direct effects on brain function, but there has been little research into the impact of systemic inflammation on the progress of dementia and neurodegenerative diseases. Now, in a study to mimic the effect of bacterial infection in people with dementia, a mouse study has revealed that that the inflammatory response to infection in mice with prior neurodegenerative disease leads to exaggerated symptoms of the infection, causes changes in memory and learning and leads to accelerated progression of dementia.

Cunningham, C. et al. In press. Systemic Inflammation Induces Acute Behavioral and Cognitive Changes and Accelerates Neurodegenerative Disease. Biological Psychiatry

http://www.eurekalert.org/pub_releases/2008-09/wt-irt091608.php

Physical frailty may be linked to Alzheimer's disease

Autopsies of the brains of 165 people who had been participants in a larger community study of chronic diseases of aging has revealed that Alzheimer's disease pathology (plaques and tangles) was associated with physical frailty in older persons regardless of whether they had dementia. The level of frailty was approximately twice as high in a person with a high level of Alzheimer’s pathology, and this was true regardless of medical history or level of physical activity. These findings raise the possibility that Alzheimer's disease may contribute to frailty or that frailty and Alzheimer's disease share a common cause. Studies show that about 7% of people over age 65 are considered frail; 45% after age 85.

Buchman, A.S., Schneider, J.A., Leurgans, S. & Bennett, D.A. 2008. Physical frailty in older persons is associated with Alzheimer disease pathology. Neurology, 71, 499-504.

http://www.eurekalert.org/pub_releases/2008-08/aaon-pfm080508.php

Thyrotropin levels associated with Alzheimer's risk in women

A clinically detectable over- or under-active thyroid has long been recognized as a potentially reversible cause of cognitive impairment. Now a large long-running study of thyrotropin (a hormone secreted by the pituitary gland that helps regulate thyroid gland function) levels has found that women with the lowest and highest levels of thyrotropin had more than double the risk of developing Alzheimer's disease. No relationship was observed between thyrotropin levels and Alzheimer's disease risk in men.

Tan, Z.S. et al. 2008. Thyroid Function and the Risk of Alzheimer Disease: The Framingham Study. Archives of Internal Medicine, 168(14), 1514-1520.

http://www.eurekalert.org/pub_releases/2008-07/jaaj-tla072408.php

Short arms and legs linked to risk of dementia

Several studies have shown that early life environment plays an important role in susceptibility to chronic disease later in life. Data from the Cardiovascular Health Cognition Study (involving 2,798 people for an average of five years) has now found that women with the shortest arm spans were 1.5 times more likely to develop dementia and Alzheimer’s disease than women with longer arm spans. For every inch longer a woman’s leg, the risk of dementia and Alzheimer’s disease was reduced by 16%. In men, only arm span was associated with a lower risk of dementia. With every increased inch in arm span, men had a 6% decrease in risk of dementia. The association between short limbs and dementia risk may be due to poor nutrition in early life, which can affect limb growth (which implies that there should be no such connection if your short limbs are due to genetics).

Szekely, C.A. et al. 2008. No advantage of Aβ₄₂-lowering NSAIDs for prevention of Alzheimer dementia in six pooled cohort studies. Neurology, 70, 2291-2298.

http://www.eurekalert.org/pub_releases/2008-05/aaon-saa042908.php

Inhaled anesthetics might increase the risk of Alzheimer's

A study using a new imaging technique has been able to see why anesthetics might cause amyloid β peptides to clump together, and whether one method of anesthesia was better than another. Previous studies have found that the inhaled anesthetics halothane and isoflurane and the intravenous anesthetic propofol encouraged the growth and clumping of Aβ in a test tube experiment. The new study found that the inhaled anesthetics caused the highest levels of Aβ aggregation, while the injected anesthetic propofol only interacted and caused aggregation at high concentrations, and thiopental did not cause the clustering of Aβ peptides even at high concentrations.

Mandal, P.K., Williams, J.P. & Mandal, R. 2007. Molecular Understanding of Aβ Peptide Interaction with Isoflurane, Propofol, and Thiopental: NMR Spectroscopic Study. Biochemistry, 46 (3), 762 –771.

http://www.eurekalert.org/pub_releases/2007-01/uopm-roa012507.php

Anesthetics a risk factor for Alzheimer’s?

The link between surgery and cognitive problems has long been noted, but it’s never been clear whether postoperative cognitive dysfunction was the result of the surgery itself or the anaesthetics. Now animal studies and test tube experiments are beginning to show that certain anaesthetics reduce the rate at which brain cells are born and develop. The latest study reveals that the inhaled anaesthetics halothane and isoflurane encourage clumping of beta amyloid protein, as does the commonly used intravenous anaesthetic propofol, at least at higher concentrations — suggesting that giving elderly patients certain general anaesthetics could increase their risk of developing Alzheimer's disease. The intravenous anaesthetic thiopental appears to have no effect on the proteins.

The study was presented at the annual Society for Neuroscience Meeting held in Atlanta, Georgia, October 14-18.

http://www.newscientist.com/channel/health/mg19225753.900-alzheimers-alert-over-anaesthetics.html
http://www.eurekalert.org/pub_releases/2006-10/ns-aao102506.php

Brain activity, drugs could affect Alzheimer's progression

Mouse studies have revealed that the activity of connections among brain cells significantly affects levels of the toxic protein beta-amyloid, suggesting that the kind of mental activity people practice or drugs they might take fo affect their risk of Alzheimer’s or the disease progression. The researchers suggest that enriched environments may increase overall synaptic activity in some brain regions and decrease it in others. Increased activity in some brain regions might result in increased susceptibility to beta-amyloid deposition if the activated neural circuits contain high levels of human APP expression. Drugs used to treat neuropsychiatric disorders directly influence neurotransmitters, and their receptors, thereby altering synaptic activity.

Cirrito, J.R. et al. 2005. Synaptic Activity Regulates Interstitial Fluid Amyloid-b Levels In Vivo. Neuron, 48, 913–922.

http://www.eurekalert.org/pub_releases/2005-12/cp-bad121505.php

New research suggests heart bypass surgery increases risk of Alzheimer's disease

Patients who have either coronary artery bypass graft surgery or coronary angioplasty are at an increased risk of developing Alzheimer's disease, according to a study involving 5,216 people who underwent coronary artery bypass graft surgery (CABG) and 3,954 people who had a percutaneous transluminal coronary angioplasty (PTCA) in 1996 and 1997. The researchers suggest the trauma to the brain during surgery is the principle cause.

Lee, T.A., Wolozin, B., Weiss, K.B. & Bednar, M.M. 2005. Assessment of the Emergence of Alzheimer's Disease Following Coronary Artery Bypass Graft Surgery or Percutaneous Transluminal Coronary Angioplasty. Journal of Alzheimer's Disease, 7 (4), 319-324.

http://www.eurekalert.org/pub_releases/2005-08/cwru-nrs082405.php

Testosterone loss may lead to Alzheimer's

A new study suggests that, like estrogen loss in older women, decreased levels of testosterone may put aging men at risk for Alzheimer's disease. The research suggests that testosterone both protects neurons from injury, and reduces levels of beta-amyloid.

Rosario, E.R., Chang, L., Stanczyk, F.Z. & Pike, C.J. 2004. Age-Related Testosterone Depletion and the Development of Alzheimer Disease. JAMA, 292, 1431-1432.

http://www.eurekalert.org/pub_releases/2004-09/uosc-alm092104.php

Coronary artery bypass surgery not a risk factor for dementia

A comparison of dementia patients with controls has found that dementia patients are no more likely than those without dementia to have had coronary artery bypass surgery.

http://www.eurekalert.org/pub_releases/2004-07/mc-cab071504.php

Minorities hardest hit by Alzheimer's disease

A study of 119 Latinos and 55 non-Latino white Alzheimer patients suggests that Latinos in the U.S. develop Alzheimer's symptoms much earlier than their white, non-Latino peers. There are several known factors which may be responsible for this apparent vulnerability in Latinos: high rates of vascular disease, leave school earlier, and less likely to use medical services or have health insurance than other Americans.

South Carolina, as the only U.S. state that keeps a comprehensive database of people with a diagnosis of Alzheimer's disease, has found that African Americans aged 55 to 64 years were more than three times as likely to have Alzheimer's as their European American counterparts. At ages 65 to 84, African Americans were more than twice as likely to have Alzheimer's. South Carolina has greater rates of obesity, diabetes, and related health problems than the rest of the country, especially amongst African Americans.

Another study has found that, in order to avoid overestimating the number of African Americans who may have early signs of Alzheimer's disease, screening tests must be adapted to cultural differences. The study involved 635 people over the age of 60. Researchers found that, using current scoring methods, African Americans scored lower on various neuropsychological tests. Even when education was taken into account, 35% of African Americans scored low enough to warrant a diagnosis of MCI, compared to only 15% of European Americans. However, when the researchers applied new, racially sensitive scoring methods they've developed, the difference in MCI rates disappeared.

Reported at The 9th International Conference on Alzheimer's Disease and Related Disorders (ICAD), July 17-22, at the Pennsylvania Convention Center in Philadelphia, Pennsylvania:

Christopher Clark – Latino Patients with AD Have An Earlier Age of Symptoms Onset Compared to Anglos (P1-041)

James Laditka – Epidemiology of Alzheimer's Disease: Race Effects, Area Variation, and Clustering (P3-132)

Marjorie Marenberg – Racial Differences in Screening of MCI in a Primary Care Population (O4-01-02)

http://www.eurekalert.org/pub_releases/2004-07/aa-mhh070704.php

Alzheimer's Association offers information about providing culturally sensitive care at http://www.alz.org//Resources/Diversity/

Low free testosterone levels linked to Alzheimer's disease in older men

A study evaluating the testosterone levels of 574 men, ages 32 to 87, who participated in the Baltimore Longitudinal Study of Aging (BLSA), found that older men with lower levels of free, or unbound, testosterone circulating in their bloodstreams were apparently at higher risk of developing Alzheimer's than their peers. This is believed to be the first study to associate low circulating blood levels of free testosterone with Alzheimer’s years before diagnosis. Previously, the same researchers had found that older men with high levels of circulating free testosterone have better visual and verbal memory and perform spatial tasks more adeptly than their peers.

Moffat, S.D., Zonderman, A.B., Metter, E.J., Kawas, C., Blackman, M.R., Harman, S.M. & Resnick, S.M. 2004. Free testosterone and risk for Alzheimer disease in older men. Neurology, 62, 188-193.

http://www.eurekalert.org/pub_releases/2004-01/naos-lft012804.php

Older news items (pre-2010) brought over from the old website

• Exercise
• Drugs

Diet

Olive oil compound may help against Alzheimer's

Oleocanthal, a naturally-occurring compound found in extra-virgin olive oil, has been found to change the size of ADDLs, impeding their ability to bind to synapses — thought to be a crucial first step in Alzheimer’s development. The compound also protected synapses from structural damage caused by ADDLs.

Pitt, J. et al. 2009. Alzheimer's-associated Aβ oligomers show altered structure, immunoreactivity and synaptotoxicity with low doses of oleocanthal. Toxicology and Applied Pharmacology, 240 (2), 189-197.

http://www.eurekalert.org/pub_releases/2009-09/mcsc-omh092909.php

Alzheimer's-fighting compounds need regular consumption

A rat study has found that the amount of polyphenols from grapeseed extract that can reach the brain is as much as 200% higher on the 10th consecutive day of feeding as compared to the first. The finding points to the value of regular consumption. Polyphenols are thought to prevent the formation of beta-amyloid protein.

Ferruzzi, M.G. et al. 2009. Bioavailability of Gallic Acid and Catechins from Grape Seed Polyphenol Extract is Improved by Repeated Dosing in Rats: Implications for Treatment in Alzheimer’s Disease. Journal of Alzheimer's Disease, 18 (1), 113-124.

http://www.eurekalert.org/pub_releases/2009-08/pu-ssh081709.php

Exercise and Mediterranean-type diet associated with lower risk for Alzheimer's

A New York study involving 1880 elderly (average age 77) is the first to investigate both exercise and diet in connection with the later development of Alzheimer’s (within a five and a half year period). Participants were asked about their activity in the two weeks prior to the interview, about the regularity and duration, as well as the quality (vigorous, moderate, light). They were also asked about their food consumption over the previous year, and their responses grouped into nine food categories, the sum of which represented a Mediterranean-type diet score. Those who were very physically active had a 33% risk reduction of Alzheimer's; those who adhered more strongly to a Mediterranean-type diet had a 40% risk reduction. Those who did both had a 60% reduction. A Mediterranean-type diet is typically characterized by high intake of fish, vegetables, legumes, fruits, cereals and monounsaturated fatty acids; relatively low intake of dairy products, meats and saturated fats; and moderate alcohol consumption.

Scarmeas, N. et al. 2009. Physical Activity, Diet, and Risk of Alzheimer Disease. Journal of the American Medical Association, 302(6), 627-637.
Full text available at http://jama.ama-assn.org/cgi/content/full/302/6/627?home

http://www.eurekalert.org/pub_releases/2009-08/cumc-eam080609.php

Mediterranean diet associated with lower risk of cognitive impairment

A study of 1,393 individuals with no cognitive problems and 482 patients with mild cognitive impairment has found that eating a Mediterranean diet was associated with less risk of developing mild cognitive impairment or of transitioning from MCI to Alzheimer's disease. Over an average of 4.5 years of follow-up, 275 of the 1,393 developed MCI. The third with the highest scores for Mediterranean diet adherence had a 28% lower risk of developing MCI compared to the third with the lowest scores, while the middle third had 17% less risk. Among the 482 with MCI, 106 developed Alzheimer's disease over an average 4.3 years of follow-up. The third with the highest scores for Mediterranean diet adherence had 48% less chance of developing Alzheimer’s and those in the middle third had 45% less chance. A number of the components of the Mediterranean diet have been associated with reduced risk of developing MCI or Alzheimer’s.

Scarmeas, N. et al. 2009. Mediterranean Diet and Mild Cognitive Impairment. Archives of Neurology, 66(2), 216-225.

http://www.eurekalert.org/pub_releases/2009-02/jaaj-mda020509.php

Moderate drinking can reduce risks of Alzheimer's dementia and cognitive decline

A review of 44 studies has concluded that moderate drinkers often have lower risks of Alzheimer's disease and other cognitive loss. Moderate alcohol consumption generally is defined as 1 drink or less per day for women and 1-2 drinks or less per day for men.

Collins, M.A. et al. 2008. Alcohol in Moderation, Cardioprotection, and Neuroprotection: Epidemiological Considerations and Mechanistic Studies. Alcoholism: Clinical and Experimental Research, Published Online 20 November

http://www.eurekalert.org/pub_releases/2008-12/luhs-mdc122908.php

Midlife coffee drinking reduces risk of dementia

A large, long-running Finnish study has found that those who were coffee drinkers at midlife had lower risk for dementia and Alzheimer’s later in life compared to those drinking no or only little coffee midlife. The lowest risk was found among moderate coffee drinkers (drinking 3-5 cups of coffee/day). Tea drinking was relatively uncommon and was not associated with dementia.

Eskelinen, M.H. et al. 2009. Midlife Coffee and Tea Drinking and the Risk of Late-Life Dementia: A Population-based CAIDE Study. Journal of Alzheimer's Disease, 16(1).

http://www.physorg.com/news151225794.html

Gingko biloba does not prevent dementia

A six-year study involving over 3000 older adults has found no reduction in the rate of dementia for those taking twice-daily 120 mg doses of Ginkgo biloba.

DeKosky, S.T. et al. Ginkgo biloba for prevention of dementia: A randomized controlled trial. JAMA, 300, 2253.

http://www.eurekalert.org/pub_releases/2008-11/jaaj-gbd111308.php
http://www.eurekalert.org/pub_releases/2008-11/wfub-gpi111808.php

Red grape seeds may help prevent Alzheimer's disease

Research into the nearly 5000 compounds contained in red wine to reveal the source of the health benefits seen from red wine has revealed that polyphenols derived from red grape seeds may be useful agents to prevent or treat Alzheimer's disease. Red grape seeds currently being developed with the name of Meganatural AZ were found to significantly reduce cognitive deterioration in genetically engineered mice, by preventing the formation of amyloid beta. The mice were given the extract before the age at which they normally develop signs of disease, suggesting the extract may help prevent or postpone the development of Alzheimer’s. The major polyphenol components in the grape seed extract product are catechin and epicatechin, which are also abundant in tea and cocoa. Unlike the polyphenol resveratrol, which has been shown to have similar effects, but requires extremely high doses, the catechins appear to be effective at much lower doses. Further research will of course be needed before human recommendations can be made.

Wang, J. et al. 2008. Grape-Derived Polyphenolics Prevent Aβ Oligomerization and Attenuate Cognitive Deterioration in a Mouse Model of Alzheimer's Disease. Journal of Neuroscience, 28, 6388-6392.

http://www.eurekalert.org/pub_releases/2008-06/tmsh-pnr061708.php
http://www.eurekalert.org/pub_releases/2008-06/sfn-sig061708.php

Vitamin E or C does not reduce risk of dementia or Alzheimer's

A five-year study involving nearly 3000 people has found that use of Vitamin C or E or both was not associated with a reduced risk of developing dementia or Alzheimer’s.

Gray, S.L. et al. 2008. Antioxidant Vitamin Supplement Use and Risk of Dementia or Alzheimer's Disease in Older Adults. Journal of the American Geriatrics Society, 56 (2), 291–295.

http://www.eurekalert.org/pub_releases/2008-02/bpl-veo020408.php

Why fish oil is good for you

Confirming previous research indicating that fish oil helps delay or prevent Alzheimer’s, a new study shows why. The study reveals that the omega-3 fatty acid DHA found in fish oil increases the production of LR11, a protein that is found at reduced levels in Alzheimer's patients and which is known to destroy the protein that forms the "plaques" associated with the disease. The study looked at both rodent brains and human brain cells. Still to be determined is what the optimal dose should be.

Ma, Q-L. et al. 2007. Omega-3 Fatty Acid Docosahexaenoic Acid Increases SorLA/LR11, a Sorting Protein with Reduced Expression in Sporadic Alzheimer's Disease (AD): Relevance to AD Prevention. Journal of Neuroscience, 27 (52), 14299 - 14307.

http://www.eurekalert.org/pub_releases/2007-12/uoc--wfo122107.php

Healthy diet lowers risk of dementia

A very large study of older adults has found that those who regularly consumed omega-3 rich oils, such as canola oil, flaxseed oil and walnut oil, reduced their risk of dementia by 60% compared to people who did not regularly consume such oils. People who ate fruits and vegetables daily also reduced their risk of dementia by 30% compared to those who didn’t regularly eat fruits and vegetables. Additionally, those who ate fish at least once a week had a 35% lower risk of Alzheimer’s and a 40% lower risk of dementia, but only if they did not carry ApoE4 gene. And finally, the study found those who didn’t have the gene but consumed an unbalanced diet characterized by regular use of omega-6 rich oils, but not omega-3 rich oils or fish, were twice as likely to develop dementia compared to those who didn’t eat omega-6 rich oils, which include sunflower or grape seed oil. The study did not find any association between consuming corn oil, peanut oil, lard, meat or wine and lowering risk of dementia.

Barberger-Gateau, P. et al. 2007. Dietary patterns and risk of dementia: The Three-City cohort study. Neurology, 69, 1921-1930.

http://www.eurekalert.org/pub_releases/2007-11/aaon-efo110607.php

Higher level of certain fatty acid associated with lower dementia risk

A nine year study of 899 participants in the Framingham Heart Study (average age 76 years) has found that those with the highest levels of an omega-3 polyunsaturated fatty acid known as docosahexaenoic acid (DHA) had a 47% lower risk of developing dementia and 39% lower risk of developing Alzheimer's. Among the participants who completed the dietary questionnaire, those in this top quartile of blood DHA levels reported that they ate an average of .18 grams of DHA a day and an average of three fish servings a week. Those in the other quartiles ate substantially less fish.

Schaefer, E.J. et al. 2006. Plasma Phosphatidylcholine Docosahexaenoic Acid Content and Risk of Dementia and Alzheimer Disease. Archives of Neurology, 63, 1545-1550.

http://www.eurekalert.org/pub_releases/2006-11/jaaj-hlo110906.php

Omega-3 fatty acids may slow cognitive decline in some patients with very mild Alzheimer's disease

Several studies have shown that eating fish, which is high in omega-3 fatty acids, may protect against Alzheimer's disease. A Swedish study has now tested whether supplements could have similar effects. Patients with mild-to-moderate Alzheimer’s who took 1.7 grams of DHA and .6g of EPA showed the same rate of cognitive decline as those taking a placebo, however, among a subgroup of 32 patients with very mild cognitive impairment, those who took the fatty acids experienced less decline in six months compared with those who took placebo. It may be that anti-inflammatory effects are an important reason for the benefit, potentially explaining why effects were seen only in those with very early-stage disease, when levels of inflammation seem to be higher.

Freund-Levi;, Y. et al. 2006. w-3 Fatty Acid Treatment in 174 Patients With Mild to Moderate Alzheimer Disease: OmegAD Study: A Randomized Double-blind Trial. Archives of Neurology, 63, 1402-1408.

http://www.eurekalert.org/pub_releases/2006-10/jaaj-ofa100506.php

Cabernet sauvignon red wine reduces the risk of Alzheimer's disease

A mouse study has found moderate consumption of the red wine Cabernet Sauvignon significantly reduced Alzheimer’s-type deterioration of spatial memory function. The Cabernet Sauvignon used contained a very low content of resveratrol, 10-fold lower than the minimal effective concentration shown to promote Aß clearance in vitro. It is suggested that, instead, the benefit occurred through promoting non-amyloidogenic processing of amyloid precursor protein. The finding supports epidemiological evidence indicating that moderate wine consumption (one drink per day for women and two for men) may help reduce the relative risk for Alzheimer’s.

Wang, J. et al. 2006. Moderate consumption of Cabernet Sauvignon attenuates Aß neuropathology in a mouse model of Alzheimer’s disease. FASEB Journal, 20, 2313-2320.

http://www.eurekalert.org/pub_releases/2006-09/tmsh-csr091806.php

Juices may reduce Alzheimer's disease risk

In a large epidemiological study, that followed 1836 Seattle residents for up to 10 years, it was found that those who drank three or more servings of fruit and vegetable juices per week had a 76% lower risk of developing Alzheimer’s disease than those who drank juice less than once a week. The benefit seemed greatest for those who carried the so-called “Alzheimer’s gene”. Previously, researchers suspected that antioxidant vitamins (vitamins C, E and -carotene) might help protect against Alzheimer's disease, but this has not been supported in recent clinical studies. Another class of antioxidant chemicals, polyphenols, are now suspected. Polyphenols generally exist primarily in the skins of fruits and vegetables and are particularly abundant in teas, juices and wines.

Dai, Q. et al. 2006. Fruit and Vegetable Juices and Alzheimer's Disease: The Kame Project. The American Journal of Medicine, 119 (9), 751-759.

http://www.eurekalert.org/pub_releases/2006-08/vumc-jmr082806.php
http://www.eurekalert.org/pub_releases/2006-08/ehs-ssf082806.php

Calorie restriction may help prevent Alzheimer's

A mouse study has found that beta-amyloid peptides can be reduced by restricting calorie intake, primarily through a low carbohydrate diet. Conversely, a high caloric intake based on saturated fat was shown to increase levels of beta-amyloid peptides. This is the first study to suggest that caloric restriction might inhibit the generation of beta-amyloid peptides, but there have been a number of studies providing evidence that high cholesterol, obesity, and other cardiovascular risk factors increase the likelihood of Alzheimer’s.

Qin, W. et al. 2006. Neuronal SIRT1 Activation as a Novel Mechanism Underlying the Prevention of Alzheimer Disease Amyloid Neuropathology by Calorie Restriction. Journal of Biological Chemistry, 281 (31), 21745 – 21754.

http://www.sciencedaily.com/releases/2006/06/060614113128.htm

Apples fight memory loss

The study involved adult and old mice (some engineered to develop Alzheimer's-like symptoms) being fed either a standard diet, a nutrient-deficient diet, or a nutrient-deficient diet supplemented with apple juice concentrate. The mice on the apple juice-supplemented diet showed an increased production of acetylcholine in their brains and performed significantly better on maze tests. The amount of consumption was comparable to humans drinking approximately two 8 oz. glasses of apple juice or eating 2-3 apples a day. The findings also suggest that the apple-supplemented diet was most helpful in the framework of an overall healthy diet. Acetylcholine levels declined in both adult and old mice on the nutrient-deficient diet.

Chan, A., Graves, V. & Shea, T.B. 2006. Apple juice concentrate maintains acetylcholine levels following dietary compromise. Journal of Alzheimer's Disease, 9(3), 287-291.

http://www.sciencedaily.com/releases/2006/08/060801225922.htm

Dietary supplements offer new hope for Alzheimer's patients

A "cocktail" of dietary supplements (omega-3 fatty acids, uridine and choline) has been found to dramatically increase the amount of membranes that form brain cell synapses in gerbils. The treatment is now in human clinical trials. It is hoped that such treatment may significantly delay Alzheimer's disease. The treatment offers a different approach from the traditional tactic of targeting amyloid plaques and tangles. Choline can be found in meats, nuts and eggs, and omega-3 fatty acids are found in a variety of sources, including fish, eggs, flaxseed and meat from grass-fed animals. Uridine, which is found in RNA and produced by the liver and kidney, is not obtained from the diet, although it is found in human breast milk.

Wurtman, R.J., Ulus, I.H., Cansev, M., Watkins, C.J., Wang L. & Marzloff, G. 2006. Synaptic proteins and phospholipids are increased in gerbil brain by administering uridine plus docosahexaenoic acid orally. Brain Research, Available online ahead of print 21 April 2006.

http://www.eurekalert.org/pub_releases/2006-04/miot-mro042706.php

Blackcurrants may protect against Alzheimer's

A cultured cell study has found that compounds in blackcurrants strongly protect neuronal cells against the types of stress caused by dopamine and amyloid-b, a peptide associated with Alzheimer's disease. Blackcurrants and boysenberries also contain anthocyanins and polyphenolics. Those that are darker (like British blackcurrants) have more anthocyanins and are likely to be more potent. Compounds from these berries are already known to act as antioxidants, but a role in neuroprotection has not been demonstrated previously.

Ghosh, D., McGhie, T.K., Zhang, J., Adaim, A. & Skinner, M. 2006. Effects of anthocyanins and other phenolics of boysenberry and blackcurrant as inhibitors of oxidative stress and damage to cellular DNA in SH-SY5Y and HL-60 cells. Journal of the Science of Food and Agriculture, in press

http://www.eurekalert.org/pub_releases/2006-01/jws-bbb011906.php

Folates more effective in limiting Alzheimer's disease risk than antioxidants, other nutrients

Analysis of data from the Baltimore Longitudinal Study of Aging has revealed that those with higher intake of folates, vitamin E and vitamin B6 had a lower risk of developing Alzheimer’s. When the three vitamins were analyzed together, only folates were associated with a significantly decreased risk. Those who had at least 400mcg of folates a day (the recommended daily allowance) had a 55% reduction in risk of developing Alzheimer’s. Unfortunately, most people who reached that level did so by taking supplements, suggesting the difficulty of doing so through diet alone. Folates are abundant in foods such as liver, kidneys, yeast, fruits (like bananas and oranges), leafy vegetables, whole-wheat bread, lima beans, eggs and milk; however, they are often destroyed by cooking or processing. No association was found between vitamin C, carotenoids (such as beta-carotene) or vitamin B-12 intake and decreased Alzheimer's risk.

Corrada, M.M., Kawas,C.H., Hallfrisch,J., Muller,D. & Brookmeyer,R. Reduced risk of Alzheimer’s disease with high folate intake: The Baltimore Longitudinal Study of Aging. Alzheimer’s & Dementia, 1 (1), 11-18.

http://www.eurekalert.org/pub_releases/2005-08/uoc--fme081105.php

Fish oil may help prevent Alzheimer's

A study involving genetically engineered mice has found that a diet high in docosahexenoic acid, or DHA — an omega-3 fatty acid found in relatively high concentrations in cold-water fish — dramatically slowed the progression of Alzheimer's, by cutting the harmful brain plaques that mark the disease. An earlier study showed that DHA protected against damage to the "synaptic" areas where brain cells communicate and enabled mice to perform better on memory tests. Food sources of omega-3 fatty acids include fish such as salmon, halibut, mackerel and sardines, as well as almonds, walnuts, soy, and DHA-enriched eggs.

Lim, G.P., Calon, F., Morihara, T., Yang, F., Teter, B., Ubeda, O., Salem, N.Jr, Frautschy, S.A. & Cole, G.M. 2005. A Diet Enriched with the Omega-3 Fatty Acid Docosahexaenoic Acid Reduces Amyloid Burden in an Aged Alzheimer Mouse Model. Journal of Neuroscience, 25(12), 3032-3040.

http://www.eurekalert.org/pub_releases/2005-03/vrcs-foh032405.php

Fewer calories may slow Alzheimer's

Restricting the diets of genetically engineered mice by 40% over 4 weeks reduced the build-up of plaques in the brain that are linked to Alzheimer's disease by 50%. It remains to be seen whether such dietary changes would similarly affect humans. Researchers are now looking to isolate the specific factors of the diet restriction which are important.

Patel, N.V., Gordon, M.N., Connor, K.E., Good, R.A., Engelman, R.W., Mason, J., Morgan, D.G., Morgan, T.E. & Finch, C.E. (in press). Caloric restriction attenuates Aβ-deposition in Alzheimer transgenic models. Neurobiology of Aging, In Press, Corrected Proof, Available online 25 November 2004.

http://www.eurekalert.org/pub_releases/2004-12/uosc-fcm121404.php

Compound in apples may help fight Alzheimer's disease

Researchers are recommending that apples may be a particularly beneficial food to protect against Alzheimer’s. A study that exposed groups of isolated rat brain cells to varying concentrations of either quercetin or vitamin C supports the theory that quercetin protects against cellular damage. A particularly good source of quercetin is apples — mainly in the skin. In general, red apples tend to have more of the antioxidant than green or yellow ones. Other foods containing high levels of quercetin include onions, which have some of the highest levels of quercetin among vegetables, as well as berries, particularly blueberries and cranberries.

The study appeared in the December 1 issue of the Journal of Agricultural and Food Chemistry.

http://www.eurekalert.org/pub_releases/2004-11/acs-ia111604.php

Tea may protect against Alzheimer’s

A study investigating the properties of coffee and green and black tea has found that both green and black tea inhibited the activity of enzymes associated with the development of Alzheimer's Disease (acetylcholinesterase and butyrylcholinesterase), but coffee had no significant effect. Green tea also obstructed the activity of beta-secretase, which plays a role in the production of protein deposits in the brain which are associated with Alzheimer's disease, and continued to have its inhibitive effect for a week, whereas black tea's enzyme-inhibiting properties lasted for only one day.

Okello, E.J., Savelev, S.U. & Perry, E.K. 2004. In vitro Anti-beta-secretase and dual anti-cholinesterase activities of Camellia sinensis L. (tea) relevant to treatment of dementia. Phytotherapy Research, 18 (8), 624-627.

http://www.eurekalert.org/pub_releases/2004-10/uonu-tci102504.php

Omega-3 fatty acid may prevent Alzheimer's disease and slow its progression

A study using genetically engineered mice has shown that a diet high in the omega-3 fatty acid DHA helps protect the brain against the memory loss and cell damage caused by Alzheimer's disease. Cheap sources of DHA include coldwater fish, like salmon, halibut, mackerel, sardines and herring. These fish consume algae, which is high in DHA. Because these fishes' oiliness makes them absorb more mercury, dioxin, PCP and other metals, however, a less risky yet more costly strategy is to consume fish oil or purified DHA supplements made from algae. Other options include DHA-rich eggs laid by chickens that eat DHA-supplemented feed.

The paper appeared in the September 2 issue of Neuron.

http://www.eurekalert.org/pub_releases/2004-09/uoc--ddp082604.php

Why diet, hormones, exercise might delay Alzheimer’s

A theory that changes in fat metabolism in the membranes of nerve cells play a role in Alzheimer's has been supported in a recent study. The study found significantly higher levels of ceramide and cholesterol in the middle frontal gyrus of Alzheimer's patients. The researchers suggest that alterations in fats (especially cholesterol and ceramide) may contribute to a "neurodegenerative cascade" that destroys neurons in Alzheimer's, and that the accumulation of ceramide and cholesterol is triggered by the oxidative stress brought on by the presence of the toxic beta amyloid peptide. The study also suggests a reason for why antioxidants such as vitamin E might delay the onset of Alzheimer's: treatment with Vitamin E reduced the levels of ceramide and cholesterol, resulting in "a significant decrease in the number of neurons killed by the beta amyloid and oxidative stress.

Cutler, R.G., Kelly, J., Storie, K., Pedersen, W.A., Tammara, A., Hatanpaa, K., Troncoso, J.C. & Mattson, M.P. 2004. Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease. PNAS, 101, 2070-5.

http://www.eurekalert.org/pub_releases/2004-02/aaft-nsm021004.php

Using vitamin E and C supplements together may reduce risk of Alzheimer's

A study involving 4,740 elderly (65 years or older) found the greatest reduction in both prevalence and incidence of Alzheimer's in those who used individual vitamin E and C supplements in combination, with or without an additional multivitamin. There was no significant benefit in using vitamin C alone, vitamin E alone, or vitamin C and multivitamins in combination.

Zandi, P.P., Anthony, J.C., Khachaturian, A.S., Stone, S.V., Gustafson, D., Tschanz, J.T., Norton, M.C., Welsh-Bohmer, K.A. & Breitner, J.C.S. 2004. Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements: The Cache County Study. Archives of Neurology, 61, 82-88.

http://www.eurekalert.org/pub_releases/2004-01/jaaj-uve011404.php

High-dose vitamin regime may help slow Alzheimer's

A preliminary study suggests that a regime of high doses of folic acid, B12 and B6 reduces levels of homocysteine in people with mild to moderate Alzheimer’s. A larger study, recruiting 400 participants from all over the U.S., is to be undertaken to assess whether such a vitamin regime can slow the progression of Alzheimer's disease. In the meantime, it is not advised that people take high doses of these vitamins, as there are possible side-effects, including peripheral nerve damage.

Aisen, P.S. et al. 2003. Effects of Rofecoxib or Naproxen vs Placebo on Alzheimer Disease Progression: A Randomized Controlled Trial. JAMA, 289, 2819-2826.

http://www.eurekalert.org/pub_releases/2003-03/gumc-cvs031403.php

Drinking wine may lower risk of dementia

Researchers in Copenhagen have followed up an analysis of drinking patterns for wine, beer and liquor of 1,709 people in the 1970s with an assessment of dementia in the 1990s, when participants were age 65 or older. 83 of the participants had developed dementia. Their alcohol intake was compared to that of those who did not develop dementia. It was found that those who drank wine occasionally had a lower risk of developing dementia, including Alzheimer's disease. Those who drank wine every day were no more or less likely to develop dementia than those who drank it less often. The study also found that occasional beer drinking was associated with an increased risk of developing dementia. It is important to note that eating habits were not investigated, and research suggests that wine drinkers may have better dietary habits than beer and liquor drinkers.

Truelsen, T., Thudium, D. & Grønbæk, M. 2002. Amount and type of alcohol and risk of dementia: The Copenhagen City Heart Study. Neurology, 59, 1313-1319.

http://www.eurekalert.org/pub_releases/2002-11/aaon-dwm110702.php

Eating fish cuts risk of dementia

Using data from a French epidemiological study of cognitive and functional aging, researchers found that those who ate fish or seafood at least once a week had a significantly lower risk of being diagnosed as having dementia (including Alzheimer’s) over the seven years follow-up. This confirms earlier findings from the Rotterdam Study, which had a much shorter follow-up (a mean of 2.1 years). There was an association between level of education and diet which partly, but not completely, explains this. It does appear that this is a benefit from eating fish / seafood, possibly from the fatty acids found in fish oils. There was no significant association between meat consumption and risk of dementia.

Barberger-Gateau, P., Letenneur, L., Deschamps, V., Pérès, K., Dartigues, J. & Renaud, S. 2002. Fish, meat, and risk of dementia: cohort study. BMJ, 325, 932-933.

http://www.eurekalert.org/pub_releases/2002-10/bmj-efc102302.php

Diet rich in foods with Vitamin E may reduce Alzheimer’s disease risk

Two studies have come out in favor of a diet rich in foods containing vitamin E to help protect against Alzheimer's disease. One study involved 815 Chicago residents age 65 and older with no initial symptoms of mental decline, who were questioned about their eating habits and followed for an average of about four years. When factors like age and education were taken into account, those eating the most vitamin E-rich foods had a lower risk of developing Alzheimer’s, provided they did not have the ApoE e4 allele. This was not true when vitamin E was taken as a supplement. Intake of vitamin C and beta carotene appeared protective, but not at a statistically significant level. The other study involved 5,395 people in the Netherlands age 55 and older who were followed for an average of six years. Those with high intakes of vitamins E and C were less likely to become afflicted with Alzheimer's, regardless of whether they had the gene variation. This association was most pronounced for current smokers, for whom beta carotene also seemed to be protective. A number of clinical trials are underway to further investigate these links.

Engelhart, M.J., Geerlings, M.I., Ruitenberg, A., van Swieten, J.C., Hofman, A., Witteman, J.C.M. & Breteler, M.M.B. 2002. Dietary Intake of Antioxidants and Risk of Alzheimer Disease. JAMA, 287, 3223-3229. Morris, M.C., Evans, D.A., Bienias, J.L., Tangney, C.C., Bennett, D.A., Aggarwal, N., Wilson, R.S. & Scherr, P.A. 2002. Dietary Intake of Antioxidant Nutrients and the Risk of Incident Alzheimer Disease in a Biracial Community Study. JAMA, 287, 3230-3237.

http://www.eurekalert.org/pub_releases/2002-06/nioa-dri062102.php
http://www.eurekalert.org/pub_releases/2002-06/pn-tsr062702.php

Folic acid possibly a key factor in preventing Alzheimer's disease

Experiments with mice bred with mutant genes that cause Alzheimer's disease found that those mice fed on a diet deficient in folate had fewer neurons in the hippocampus ( a brain region critical for learning and memory that is destroyed as plaques accumulate during Alzheimer’s disease), and elevated levels of homocysteine. Researchers suspect that increased levels of homocysteine in the brain caused damage to the DNA of nerve cells in the hippocampus. In the mice fed an adequate amount of folate, nerve cells in this brain region were able to repair the damage. But in those mice fed a folate-deficient diet, nerve cells were unable to repair this damage. A human study is being planned.
Green leafy vegetables, citrus fruits and juices, whole wheat bread and dry beans are good sources of folate. In the U.S., since 1998, the Food and Drug Administration has required the addition of folic acid to enriched breads, cereals, flours, corn meals, pastas, rice, and other grain products.

Kruman, I.I., Kumaravel, T.S., Lohani, A., Pedersen, W.A., Cutler, R.G., Kruman, Y., Haughey, N., Lee, J., Evans, M. & Mattson, M.P. 2002. Folic Acid Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons and Sensitize Them to Amyloid Toxicity in Experimental Models of Alzheimer's Disease. Journal of Neuroscience, 22, 1752-1762.

http://www.eurekalert.org/pub_releases/2002-03/nioa-fap030102.php

Physical exercise & fitness

Reduced muscle strength associated with Alzheimer's risk

A study involving 970 older adults (average age 80.3) has found that over the average 3.6 years follow-up period, those with weaker muscles had a higher risk of developing Alzheimer’s. For each one-unit increase at the beginning of the study, older adults had about a 43% decrease in the risk of developing Alzheimer's disease during follow-up (strength scores ranged from -1.6 to 3.3 units). Those in the top 10% had about a 61% reduced risk of developing Alzheimer's compared with those in the bottom 10%. The association remained even after factors such as body mass index and physical activity level were accounted for. The association also was found with mild cognitive impairment.

Boyle, P. A., Buchman, A. S., Wilson, R. S., Leurgans, S. E., & Bennett, D. A. (2009). Association of Muscle Strength With the Risk of Alzheimer Disease and the Rate of Cognitive Decline in Community-Dwelling Older Persons. Arch Neurol, 66(11), 1339-1344.

http://www.eurekalert.org/pub_releases/2009-11/jaaj-sb110509.php

Physical fitness improves memory in seniors

A study of 165 older adults (59-81) has found a significant association between physical fitness and performance on certain spatial memory tests. Fitness was also strongly correlated with hippocampus size. Although rodent studies have shown that exercise increases hippocampus size and spatial memory, this is the first study to show that in humans. The findings provide more evidence for the benefits of physical exercise in preventing memory loss in older adults.

Erickson, K.I. et al.  2009. Aerobic fitness is associated with hippocampal volume in elderly humans. Hippocampus, Published online 2 January

http://www.eurekalert.org/pub_releases/2009-02/uoia-pfi022409.php

Moderate exercise helps mild cognitive impairment

An Australian study involving 138 older adults (50 years and over) with mild cognitive impairment, has found that those who undertook to achieve 2 ½ hours of physical activity each week (three 50 minute sessions), ranging from walking, ballroom dancing to swimming, for a six month period, continually out-scored the control group on cognitive tests during the 18 month testing period — showing that memory improvement was still evident a year after the supervised exercise period.

Lautenschlager, N.T. et al. 2008. Effect of Physical Activity on Cognitive Function in Older Adults at Risk for Alzheimer Disease: A Randomized Trial. Journal of the American Medical Association, 300(9), 1027-1037.

http://www.eurekalert.org/pub_releases/2008-09/ra-wtp090108.php
http://www.eurekalert.org/pub_releases/2008-09/uom-aow090108.php
http://www.eurekalert.org/pub_releases/2008-09/jaaj-emh082808.php

Exercise may slow brain shrinkage in early Alzheimer's

A study of 121 people age 60 and older, of whom 57 were in the early stages of Alzheimer's disease, has found that those with early Alzheimer's disease who were less physically fit (measured by cardiorespiratory fitness) had four times more brain shrinkage when compared to normal older adults than those who were more physically fit. The findings suggest the value of physical fitness in slowing down the progression of Alzheimer's disease. The association existed even after age, gender, severity of dementia, physical activity and frailty were accounted for. There was no relationship between higher fitness levels and brain changes in the group of people without dementia.

Burns, J.M. et al. 2008. Cardiorespiratory fitness and brain atrophy in early Alzheimer disease. Neurology, 71, 210-216.

http://www.eurekalert.org/pub_releases/2008-07/aaon-emp070808.php

Walking and moderate exercise help prevent dementia

A four-year study involving 749 older adults has found that the top one-third of participants who exerted the most energy in moderate activities such as walking were significantly less likely to develop vascular dementia than those people in the bottom one-third of the group. Contrary to some reports, no such association was found with Alzheimer’s disease.

Ravaglia, G. et al. 2007. Physical activity and dementia risk in the elderly. Findings from a prospective Italian study. Neurology, published online ahead of print December 19

http://www.eurekalert.org/pub_releases/2007-12/aaon-wam121107.php

Good physical function linked to Alzheimer's delay

A study following 2,288 older adults for six years found that those whose physical function was higher at the start of the study were three times less likely to develop dementia than were those whose physical function was lower.

Wang, L., Larson, E.B., Bowen, J.D. & van Belle, G. 2006. Performance-Based Physical Function and Future Dementia in Older People. Archives of Internal Medicine, 166, 1115-1120.

http://www.eurekalert.org/pub_releases/2006-05/ghcc-gpf051806.php

Exercise protects against Alzheimer's

A study following 1,740 seniors (aged 65 and older) over a six-year period, found that those who exercised three or more times a week had a 30 — 40% lower risk for developing dementia compared with those who exercised fewer than three times per week. Even modest amounts, such as walking 15 minutes a day, appear beneficial, and the more frail the person was, the more they benefited from regular exercise.

Larson, E.B., Wang, L., Bowen, J.D., McCormick, W.C., Teri, L., Crane, P., & Kukull, W. 2006. Exercise Is Associated with Reduced Risk for Incident Dementia among Persons 65 Years of Age and Older. Annals of Internal Medicine, 144 (2), 73-81.

http://www.eurekalert.org/pub_releases/2006-01/ghcc-eil011006.php

Exercise slows development of Alzheimer's-like brain changes in mice

Population-based studies have provided evidence that various lifestyle interventions might help slow the onset and progression of Alzheimer’s. A mouse study now provides a clue how that might work. Physical activity enhanced the learning ability of mice genetically engineered to develop amyloid plaques and decreased the level of plaque-forming beta-amyloid protein fragments in their brains. The mice were divided into mice with access to running wheels or no access. The findings are supported by another recent study that found that beta-amyloid levels decreased in the brains of another kind of transgenic mice when they were housed in groups and in environments that were enriched with running wheels, colored tunnels, and toys.

Adlard, P.A., Perreau, V.M., Pop, V. & Cotman, C.W. 2005. Voluntary Exercise Decreases Amyloid Load in a Transgenic Model of Alzheimer's Disease. Journal of Neuroscience, 25, 4217-4221.

http://www.eurekalert.org/pub_releases/2005-04/nioa-esd042605.php

 

Drugs

Estrogen use before 65 linked to reduced risk of Alzheimer's disease

Data from the Women’s Health Initiative Memory Study looked at prior hormone use in 7,153 healthy women ages 65-79 before they enrolled in the WHI Memory Study, and followed their cognitive health over an average of five years. In that time, 106 of the women developed Alzheimer’s disease or dementia. The study found women who used any form of estrogen hormone therapy before the age of 65 were nearly 50% less likely to develop Alzheimer’s disease or dementia than women who did not use hormone therapy before age 65, but women who began estrogen-only therapy after the age of 65 had roughly a 50% increased risk of developing dementia. The risk jumped to nearly double for women using estrogen-plus-progestin hormone therapy.

The findings were presented at the American Academy of Neurology’s 59th Annual Meeting in Boston, April 28 – May 5, 2007.

http://www.eurekalert.org/pub_releases/2007-05/aaon-eub041007.php

Low dose aspirin does not protect women against cognitive decline

Evidence that aspirin and other anti-inflammatory drugs may protect against dementia has been inconclusive. Now a large, long-running study involving 6,377 women aged 65 years or more, over ten years, has found that those who took low dose aspirin (100 mg on alternate days) performed at similar levels to a placebo group on cognitive tests. However, there was evidence of benefit in one very specific area of cognition: category fluency.

Kang, J-E., Cirrito, J.R., Dong, H., Csernansky, J.G. & Holtzman, D.M. 2007. Acute stress increases interstitial fluid amyloid-beta via corticotropin-releasing factor and neuronal activity. Proceedings of the National Academy of Science, 104 (25), 10673-10678.

http://www.eurekalert.org/pub_releases/2007-04/bmj-lda042607.php

Common painkillers may help protect against Alzheimer’s disease

Observations that people who take anti-inflammatory medications over several years have a lower risk of later developing Alzheimer's disease have received support from an exciting new study which has revealed that common over-the-counter pain medications (such as ibuprofen and naproxen) bind to amyloid plaques, and may help dissolve existing plaques and prevent the formation of new ones. Amyloid plaques are one of the definitive hallmarks of Alzheimer's disease.

Agdeppa, E.D., Kepe, V., Petri, A., Satyamurthy, N., Liu, J., Huang, S.-C., Small, G.W., Cole, G.M. & Barrio, J.R. 2003. In vitro detection of (S)-naproxen and ibuprofen binding to plaques in the Alzheimer's brain using the positron emission tomography molecular imaging probe 2-(1-{6-[(2-[¹⁸F]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene)malononitrile, Neuroscience, 117(3), 723-730.

http://www.eurekalert.org/pub_releases/2003-03/uoc--urd031203.php

Regular long-term use of aspirin may reduce the risk of Alzheimer’s

A large-scale study of 5,092 older adults has found that regular use of aspirin and other non-steroidal anti-inflammatory drugs may reduce the incidence of dementia in elderly people, but only when taken for more than two years, and provided the use occurred well before the onset of dementia.

Zandi, P.P., Anthony, J.C., Hayden, K.M., Mehta, K., Mayer, L. & Breitner, J.C.S. 2002. Reduced incidence of AD with NSAID but not H₂ receptor antagonists: The Cache County Study. Neurology, 59, 880-886.

http://www.eurekalert.org/pub_releases/2002-09/aaon-get091702.php

Older news items (pre-2010) brought over from the old website

Effective new cognitive screening test for detection of Alzheimer's

A new cognitive test for detecting Alzheimer's has been developed, and designed to be suitable for non-specialist use. The TYM ("test your memory") involves 10 tasks including ability to copy a sentence, semantic knowledge, calculation, verbal fluency and recall ability. It has been tested on 540 healthy individuals and 139 patients with diagnosed Alzheimer's or mild cognitive impairment. Healthy controls completed the test in an average time of five minutes and gained an average score of 47 out of 50, compared to 45 for those with mild cognitive impairment, 39 for those with non-Alzheimer dementias and 33 for those with Alzheimer’s. Among controls, the average score was not affected by age until after 70, when it showed a small decline. There were no gender or geographical background differences in performance. The TYM detected 93% of patients with Alzheimer's, compared to only 52% by the widely used mini-mental state examination.

Brown, J. et al. 2009. Self administered cognitive screening test (TYM) for detection of Alzheimer’s disease: cross sectional study. BMJ, 338:b2030, doi: 10.1136/bmj.b2030
Full text available here.

Early identification of dementia increasingly difficult

A study comparing nondemented 70-year-olds examined in the early 1970s with nondemented 70-year-olds examined in the year 2000 has revealed that those who were examined in 2000 scored much higher on non-memory cognitive tests than those examined 30 years earlier — indicating that such tests can no longer be used to predict future dementia. Moreover, although memory loss was a predictor for later development of dementia, it wasn’t conclusive —not everybody with poor memory developed dementia. This was particularly true of the very old (85 year olds).

Sacuiu, S.F. 2009. Prodromal Cognitive Signs of Dementia. Doctoral thesis from Sahlgrenska Academy, University of Gothenburg. http://gupea.ub.gu.se/dspace/handle/2077/19395

http://www.eurekalert.org/pub_releases/2009-05/uog-eio_1052009.php

Degree of test variability improves dementia diagnosis

A study of nearly 900 older adults has found that the degree of variability in performance across neuropsychological tests, measured within a person, improved the prediction of dementia above and beyond one's level of performance on each test alone.

Holtzer, R. et al. 2008. Within-Person Across-Neuropsychological Test Variability and Incident Dementia. JAMA, 300(7), 823-830.

http://www.eurekalert.org/pub_releases/2008-08/aeco-set081908.php

New criterion may improve identification of dementia risk in highly educated older adults

A shift in the cutoff point on the widely used cognitive screening tool, the mini-mental state examination (MMSE), is suggested for highly educated older adults, in order to more effectively assess the risk of dementia.

Bryant, S.E. et al. 2008. Detecting Dementia With the Mini-Mental State Examination in Highly Educated Individuals. Archives of Neurology, 65 (7), 963-967.

http://www.eurekalert.org/pub_releases/2008-07/jaaj-ncm071008.php

New 'everyday cognition' scale tracks how older adults function in daily life

A new, carefully validated questionnaire called Everyday Cognition (ECog) has been developed by seven psychologists. The 39-question screening tool is designed to enable mild functional problems in older adults to be quickly and easily identified. The questionnaire needs to be filled out by someone who knows an older adult well, such as a spouse, adult child, or close friend. It looks at everyday function in seven key cognitive domains: memory, language, semantic (factual) knowledge, visuospatial abilities, planning, organization and divided attention. The test has been shown to be sensitive to early changes present in Mild Cognitive Impairment, and unlike other cognitive tests, does not appear to be strongly influenced by education level. The test even differentiated between people diagnosed with mild impairment in memory only and those mildly impaired in several areas.

Farias, S.T. et al. 2008. The Measurement of Everyday Cognition (ECog): Scale Development and Psychometric Properties. Neuropsychology, 22 ( 4), 531-544.

http://www.eurekalert.org/pub_releases/2008-07/apa-nc062408.php

Simple test predicts 6-year risk of dementia

A 14-point index combining medical history, cognitive testing, and physical examination — a simple test that can be given by any physician — has been found to predict a person’s risk for developing dementia within six years with 87% accuracy. As measured by the index, the risk factors for developing dementia are an age of 70 or older, poor scores on two simple cognitive tests, slow physical functioning on everyday tasks such as buttoning a shirt or walking 15 feet, a history of coronary artery bypass surgery, a body mass index of less than 18, and current non-consumption of alcohol. The results do need to be validated in other populations — for example, they have not yet been tested on Hispanics or Asian-Americans.

The tests were described in a presentation at the 2007 International Conference on Prevention of Dementia, in Washington, DC.

http://www.eurekalert.org/pub_releases/2007-06/uoc--stp060707.php

Personality changes may help detect Lewy bodies dementia

Dementia with Lewy bodies is the second most common neurodegenerative cause of dementia. It shares characteristics with both Alzheimer's and Parkinson's disease, but some medications used to treat Alzheimer's patients are potentially dangerous for people with dementia with Lewy bodies. Early diagnosis is therefore important. A new study has found that people with dementia with Lewy bodies often display passive personality changes some time before cognitive deficits are evident, offering hope that a simple personality test might help diagnosis.

Galvin, J.E., Malcom, H., Johnson, D. & Morris, J.C. 2007. Personality traits distinguishing dementia with Lewy bodies from Alzheimer disease. Neurology, 68, 1895-1901.

http://www.eurekalert.org/pub_releases/2007-05/aaon-pcm052107.php

New dementia screening tool detects early cognitive problems

A new screening tool for dementia — the Saint Louis University Mental Status Examination (SLUMS) — appears to work better in identifying mild cognitive problems in the elderly than the commonly used Mini Mental Status Examination — particularly for the more educated patients. It takes a clinician about seven minutes to administer the SLUMS, which supplements the Mini Mental Status Examination by asking patients to perform tasks such as doing simple math computations, naming animals, recalling facts and drawing the hands on a clock. The SLUMS is available at this link http://medschool.slu.edu/agingsuccessfully/pdfsurveys/slumsexam_05.pdf

Tariq, S.H. et al. 2006. Comparison of the Saint Louis University Mental Status Examination and the Mini-Mental State Examination for Detecting Dementia and Mild Neurocognitive Disorder—A Pilot Study. American Journal of Geriatric Psychiatry, 14, 900-910.

http://www.eurekalert.org/pub_releases/2006-11/slu-nds103006.php

More sensitive tests for predicting Alzheimer's

The first study used data from 119 participants in the Longitudinal Aging Study Amsterdam. The memory test scores of those who two years later developed Alzheimer's were compared with the scores of those who stayed healthy. Three tests were very good at predicting who would later develop Alzheimer's: a Paired-Associate Learning Test, which cued participants to recall five semantically related and five semantically unrelated pairs of words; a Perceptual Identification Task, which measured how fast participants read aloud words briefly presented on a computer screen; a Visual Association Test, which cued participants to recall six line drawings of common objects that had been presented earlier in an illogical interaction with another object or cue. On the word-pair memory test, people destined to develop Alzheimer's disease didn't do any better when words were related than when they weren't, suggesting they’d already lost deep semantic knowledge. On the word-reading test, word repetition didn't help high-risk participants to perform better, a sign that implicit learning was impaired. The popular Mini Mental Status Exam (MMSE), a test mainly sensitive to episodic memory, was not as good a predictor.
In the second study, a dichotic listening task, which measures how well people process information when they hear one thing in the left ear and another in the right ear, was found to also be predictive of Alzheimer’s, confirming that people have problems with selective attention very early in the disease.

Spaan, P.E.J., Raaijmakers, J.G.W. & Jonker, C. 2005. Early Assessment of Dementia: The Contribution of Different Memory Components. Neuropsychology, 19 (5).

Duchek, J.M. & Balota, D.A. 2005. Failure to Control Prepotent Pathways in Early Stage Dementia of the Alzheimer's Type: Evidence from Dichotic Listening. Neuropsychology, 19 (5).

http://www.eurekalert.org/pub_releases/2005-09/apa-pfm092105.php

Early warning signs of Alzheimer's show up years before official diagnosis

A meta-analysis of 47 studies of Alzheimer's disease has revealed that people can show early warning signs across several cognitive domains years before they are officially diagnosed, confirming that Alzheimer's causes general deterioration and tends to follow a stable preclinical stage with a sharp drop in function. People at the preclinical stage showed marked preclinical deficits in global cognitive ability, episodic memory, perceptual speed, and executive functioning; along with somewhat smaller deficits in verbal ability, visuospatial skill, and attention. There was no preclinical impairment in primary memory. There is no clear qualitative difference between the normal 75-year old and a preclinical Alzheimer’s sufferer; instead it seems that the normal elderly person, the preclinical Alzheimer’s person, and the early clinical Alzheimer’s patient represent three instances on a continuum of cognitive capabilities.

Bäckman, L., Jones, S., Berger, A-K. & Laukka, E.J. 2005. Cognitive impairment in preclinical Alzheimer's disease: A meta-analysis. Neuropsychology, 19 (4).

http://www.eurekalert.org/pub_releases/2005-07/apa-ews072505.php

More sensitive test norms better predict who might develop Alzheimer's disease

Early diagnosis of Alzheimer's is becoming more important with new medical and psychological interventions that can slow (but not stop) the course of the disease. Given this, it is suggested that more sensitive testing may be necessary for highly intelligent people, who, on average, show clinical signs of Alzheimer's later than the general population. Once they show such signs, they decline much faster. A study of 42 older people with IQ's of 120 or more, used two different test norms to forecast problems: the standard norm, derived from a large cross-section of the population, or an adjusted high-IQ norm that measured changes against the individual's higher ability level. The raised cutoffs predicted that 11 of the 42 individuals were at risk for future decline – compared with standard cutoffs, which indicated they were normal. True to the former prediction, three and a half years later, nine of those 11 people had declined. Six of those went on to develop mild cognitive impairment (MCI), a transitional illness from normal aging to a dementia (of which one type is Alzheimer's). Five of these individuals have since received a diagnosis of Alzheimer's disease, two years after this study was submitted. It is also suggested that, at the other end of the scale, those with below-average intelligence have the potential for being misdiagnosed as 'demented' when they are not, and the norms should be adjusted downwards accordingly.

Rentz, D.M., Huh, T.J., Faust, R.R., Budson, A.E., Scinto, L.F.M., Sperling, R.A. & Daffner, K.R. 2004. Use of IQ-Adjusted Norms to Predict Progressive Cognitive Decline in Highly Intelligent Older Individuals. Neuropsychology, 18 (1).

http://www.eurekalert.org/pub_releases/2004-01/apa-mst122903.php

New method of distinguishing Alzheimer's from Lewy body dementia

Looking at specific changes in alertness and cognition may provide a reliable method for distinguishing Alzheimer's from dementia with Lewy bodies (DLB) and normal aging. Four characteristics significantly distinguished patients with DLB from persons with Alzheimer’s and normal elderly controls: daytime drowsiness and lethargy despite getting enough sleep the night before; falling asleep two or more hours during the day; staring into space for long periods and episodes of disorganized speech. "For the normal elderly control group, one or two of these behaviors was found in only 11 percent of the group. For the patients with AD, one or two of these behaviors were not uncommon, but over 63% of the patients with DLB had three or four of these behaviors.” DLB accounts for as much as 20 to 35% of the dementia seen in the United States.

Ferman, T.J., Smith, G.E., Boeve, B.F., Ivnik, R.J., Petersen, R.C., Knopman, D., Graff-Radford, N., Parisi, J. & Dickson, D.W. 2004. DLB fluctuations: Specific features that reliably differentiate DLB from AD and normal aging. Neurology, 62,181-187.

http://www.eurekalert.org/pub_releases/2004-01/ama-nmo010804.php

Brief telephone questionnaire screens for early signs of dementia

Researchers have developed a brief telephonic questionnaire that helps distinguish between persons with early signs of dementia and persons with normal cognitive function. The questionnaire provides a way to reach out to persons with dementia whose impairment otherwise may go undetected until substantial cognitive deterioration has occurred. The questionnaire consists of a test of delayed recall and 2 questions that ask whether the person needs help with remembering to take medications or with planning a trip for errands. It is estimated that of 100 people who score positive on this test, 42 will actually have cognitive impairment. In other words, this does not provide a diagnosis of Alzheimer’s, but provides evidence that further evaluation is required. The rate of false positives compares favorably to other types of screening tests. A further study is underway to confirm the validity and reliability of the test.

Fillit, H. et al. 2003. A Brief Telephonic Instrument to Screen for Cognitive Impairment in a Managed Care Population. Journal of Clinical Outcomes Management, , 419-429.

http://www.eurekalert.org/pub_releases/2003-09/twc-btq091603.php

Verbal memory tests predict dementia

The Longitudinal Aging Study Amsterdam tested the memories of a large group of elderly people on two occasions, two years apart. Performance on the memory tests was then compared between those who developed dementia during those two years and those who did not. It was found that those who later were found to have dementia were scarcely better at remembering word pairs clearly linked in meaning (for example, pipe - cigar) than word pairs without such a link (for example nail - butter), on the first test. (those who not have dementia two years later did, as is usual, benefit from such a link in meaning). In addition, those in the early stage of dementia did not benefit from the repeated presentation of words. The results suggest a means by which elderly people in the early stages of dementia can be identified, which is important because the drugs used to inhibit dementia only work in the earliest stages of the disease.

This was revealed in doctoral research by the neuropsychologist Pauline Spaan from the University of Amsterdam.

http://www.eurekalert.org/pub_releases/2003-01/nofs-mtp012403.php

Verbal memory test best indicator of who will have Alzheimer's disease

A meta-analysis of 31 studies involving a total of 1,144 Alzheimer's patients and 6,046 healthy controls, supports the use of the California Verbal Learning Test in predicting future Alzheimer’s type dementia. Long delay recall and percent recall were the best predictors, with executive function type measures also being predictive but less so than both the long and short delay memory tests. Changes in the hippocampus were the best volumetric or neuroimaging measure but in general volumetric measures were less sensitive to preclinical stages of the dementia than were the neuropsychological tests. It should be noted that a decline in various types of memory, especially verbal episodic memory, is also observable in normal elderly; the crucial factor in determining a pre-dementia state lies in the size of the memory deficit.

Zakzanis, K.K. & Boulos, M.I. 2002. A Meta-Analysis of ApoE Genotype and Neuropsychologic and Neuroanatomic Changes in Preclinical Alzheimer's Disease. Presentation at the 110th Annual Convention of the American Psychological Association (APA) on August 25.

http://www.eurekalert.org/pub_releases/2002-08/apa-vmt081302.php

Early diagnosis of Alzheimer's

An analysis of data from 40 participants enrolled in a long-term study at the UCSD Alzheimer’s Disease Research Center (ADRC) found that "paper-and-pencil" cognitive skills tests administered to normal subjects averaging 75 years of age contained early signs of cognitive decline in those subjects who later developed Alzheimer’s disease. All participants were symptom-free when they took the test. The differences were quite subtle - only some performance measures were affected.

Jacobson MW, Delis DC, Bondi MW, Salmon DP. Do neuropsychological tests detect preclinical Alzheimer's disease: Individual-test versus cognitive-discrepancy score analyses. Neuropsychology. 2002;16(2):132–139.

http://www.eurekalert.org/pub_releases/2002-04/uoc--trs040502.php

Older news items (pre-2010) brought over from the old website

Impact of Alzheimer's gene on healthy brains

And another new imaging analysis technique has cast light on the impact of the Alzheimer’s gene ApoE4 in healthy brains. Healthy older adults with the gene were found to have reduced cognitive performance, decreased brain volume in the hippocampus and amygdala, and decreased white matter integrity in the left parahippocampal gyrus.

Honea, Robyn A., Eric Vidoni, Amith Harsha and Jeffrey M. Burns. Impact of APOE on the Healthy Aging Brain: A Voxel-Based MRI and DTI Study. J Alzheimers Dis 18:3, 553-564.

http://www.eurekalert.org/pub_releases/2009-11/ip-nna111709.php

Three new genes associated with Alzheimer's found

Only one gene, ApoE4, has been associated with the non-familial (common) form of Alzheimer’s. Now the largest ever Alzheimer's genome-wide association study involving 16,000 individuals, has found three more. CLU or ApoJ (which produces a protective protein called clusterin or apolipoprotein J), PICALM (important at synapses and involved in transporting molecules within and into nerve cells), and CR1. Both CLU and CR1 have previously been implicated in the clearance of amyloid beta peptide. CLU is encoded on chromosome 8, CR1 on chromosome 1, and PICALM on chromosome 11.

Harold, D. et al. 2009. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease. Nature Genetics, 41, 1088–1093. Lambert, J-C et al. 2009. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease. Nature Genetics, 41, 1094-1099.

http://www.eurekalert.org/pub_releases/2009-09/art-lea090309.php

Carriers of Alzheimer's gene show different brain activity as young adults

Possession of the ApoE4 gene variant associated with Alzheimer’s risk is found in about a quarter of the population, and has been shown to be associated with differences in the hippocampus in middle-aged and elderly healthy carriers. Now a new study of 36 younger adults (20-35) has revealed that differences in brain activity patterns between carriers and non-carriers are also evident at this stage, not only when performing a memory task, but even when the brain was at rest. Carriers of the gene had more brain activity in the hippocampus during the memory task, and more activity in the default mode network during rest. The findings support a theory that the brain's memory function may gradually wear itself out in those who go on to develop Alzheimer's.

Filippini, N. et al. 2009. Distinct patterns of brain activity in young carriers of the APOE-ε4 allele. Proceedings of the National Academy of Sciences, 106, 7209-7214.

http://www.eurekalert.org/pub_releases/2009-04/icl-yaa040609.php

Having a parent with dementia may affect memory in midlife

A study of 715 participants from the second generation of the Framingham Heart Study (average age 59) has found that, among those with the ApoE ε4 gene, those who had parents with dementia scored significantly worse on tests of verbal memory and visual memory than persons who did not have parents with dementia. The impairment was strongest in those whose parents had Alzheimer’s (rather than other forms of dementia), and in them was equivalent to around 15 years of brain aging. The effect of parental dementia was not found in those who didn’t have the ApoE ε4 gene.

Debette, S. et al. 2009. Parental Dementia and Alzheimer Disease Are Associated with Poorer Memory in Middle-Aged Adults: The Framingham Offspring Study. Presented April 29 at the American Academy of Neurology's 61st Annual Meeting in Seattle, Washington.

http://www.eurekalert.org/pub_releases/2009-02/bu-brf021209.php
http://www.eurekalert.org/pub_releases/2009-02/aaon-hap021009.php

Memory gene linked to late-onset Alzheimer's

Following the finding that carriers of one variant (the T-allele) of the KIBRA gene performed better on memory tests compared to those carrying the C-allele, researchers have now found that carriers of the T-allele have a 25% lower risk of developing Alzheimer's disease. The conclusion is supported by three studies. A study of 702 deceased persons diagnosed with Alzheimer's, and 1,026 living and deceased persons with and without Alzheimer's, found that non-carriers of the KIBRA T-allele had increased risk of late-onset Alzheimer¹s. A study of brain tissue from 47 deceased individuals found that KIBRA, and a subset of other molecules directly interacting with it, were significantly altered in regions of the brain involved in Alzheimer's disease pathology, but not in a region of the brain typically unaffected -- the primary visual cortex. PET scans of 136 individuals aged 47 to 68, with close relatives diagnosed with Alzheimer's, of whom half carried the T-allele, found that non-carriers exhibited, on average, less metabolic activity in key brain regions known to be altered in the earliest stages of the disease. Similar findings have been found when looking at the epsilon 4 allele of apolipoprotein E (the ‘Alzheimer’s gene’). In the current study, the effects of this allele were controlled for.

Corneveaux, J.J. et al. In press. Evidence for an association between KIBRA and late-onset Alzheimer's disease. Neurobiology of Aging

http://www.eurekalert.org/pub_releases/2008-09/ttgr-itt091508.php

Healthy children of Alzheimer patients show early brain changes

A study of 28 neurologically-normal subjects, between ages 45 and 65, of whom 12 carried the ‘Alzheimer’s gene’ APOE-4, has found that although there was no significant difference in educational level or neuropsychological performances, those who didn’t carry the gene had significantly better functional connectivity between the hippocampus and the posterior cingulated cortex.

The findings were presented at the Alzheimer's Association International Conference on Alzheimer's disease in Chicago, July 29.

http://www.eurekalert.org/pub_releases/2008-07/mcow-nsf072308.php

Women more likely to have memory problems in very old age

Dementia risk for both men and women increases from age 65 to 85, but a study of about 900 people age 90 and older has found that women were nearly twice as likely to have dementia in their 90s compared to men. The results also showed that the likelihood of having dementia doubled every five years in women but not in men. Women with a higher education appeared to be as much as 45% less likely to have dementia compared to women with less education.

Corrada, M.M. et al. 2008. Prevalence of dementia after age 90: Results from The 90+ Study. Neurology, 71 (5), 337-343.

http://www.eurekalert.org/pub_releases/2008-07/aaon-amo062408.php

Gene variation linked to earlier onset of Alzheimer's symptoms

Another genetic variation has been found for Alzheimer’s disease. Unlike the ‘Alzheimer’s gene’ APOe4, which is linked to the rare early-onset form, this gene variant is linked to early presentation in people afflicted with the more common, late-onset form. Rather than increasing the risk of Alzheimer’s, the gene increases the vulnerability of carriers to the effects of amyloid plaques, so that symptoms become evident earlier. The gene codes for the tau protein found in neurofibrillary tangles. Previous studies have had inconsistent results, but the new study has dealt with previous difficulties.

Kauwe, J.S.K. et al. 2008. Variation in MAPT is associated with cerebrospinal fluid tau levels in the presence of amyloid-beta deposition. Proceedings of the National Academy of Sciences, 105 (23), 8050-8054.

http://www.eurekalert.org/pub_releases/2008-06/wuso-gvl060608.php

Maternal inheritance more importance than paternal for Alzheimer's risk?

In an intriguing preliminary study comparing brain metabolism among cognitively normal people who have a father, a mother, or no relatives with Alzheimer’s disease, researchers have found that only those with an affected mother have reduced brain metabolism in the same brain regions as Alzheimer’s patients.

Mosconi, L. et al. 2007. Maternal family history of Alzheimer's disease predisposes to reduced brain glucose metabolism. PNAS, 104, 19067-19072.

http://www.eurekalert.org/pub_releases/2007-11/nyum-aml110607.php

Familial link between Parkinson's and dementia

A study of relatives of patients with Parkinson’s disease provides evidence that relatives of patients with Parkinson’s disease (primarily younger age at onset Parkinson’s) have an increased risk of cognitive impairment or dementia.

Rocca, W.A. et al. 2007. Risk of Cognitive Impairment or Dementia in Relatives of Patients With Parkinson Disease. Archives of Neurology, 64(10),1458-1464.

http://www.eurekalert.org/pub_releases/2007-10/jaaj-rop100407.php

High stress and genetic risk factor lead to increased memory decline

A study involving 91 older, healthy subjects (mean age 78.8 years) has found that those low on stress (low levels in cortisol) or without the APOE-ε4 gene performed better on memory measures than those with high stress or those with the APOE-ε4 gene. Those who had the gene and had high stress levels showed the greatest memory impairment.

Peavy, G.M. et al. 2007. The Effects of Prolonged Stress and APOE Genotype on Memory and Cortisol in Older Adults. Biological Psychiatry, 62 (5), 472-478.

http://www.eurekalert.org/pub_releases/2007-08/e-naf082707.php

New Alzheimer's gene

A study comparing more genetic markers in the DNA of people with and without Alzheimer’s disease than ever before has revealed a new gene that may increase a person’s risk for developing Alzheimer’s disease. The gene — GAB2 — appears to modify an individual’s risk when associated with other genes, including APOE4. It’s suggested that the healthy form of the GAB2 gene protects brain cells from developing tangles. If confirmed, this discovery could provide a target for future therapeutic drugs.

Reiman, E.M. et al. 2007. GAB2 Alleles Modify Alzheimer's Risk in APOE e4 Carriers. Neuron, 54, 713-720.

http://www.eurekalert.org/pub_releases/2007-06/ttgr-rti060107.php

Study examines genetic risk factors for Alzheimer's disease

A Welsh study that tested more than 17,000 gene variants in 4,000 volunteers has found evidence for several genes contributing to Alzheimer’s disease, the most interesting one being GALP, thought to affect the development of tangles within brain cells.

The findings will be published in a future issue of Human Molecular Genetics.

http://www.eurekalert.org/pub_releases/2007-03/cu-seg030507.php

Two-fold role of Alzheimer’s genes?

The genes responsible for an inherited form of Alzheimer's disease — two genes known as presenilins — are primarily known for their role as an enzyme that cleaves amyloid precursor protein (APP) to form amyloid ß-peptide, which function has a direct connection to Alzheimer’s, and consequently has been the focus of attention. However, new research indicates that these genes also may control the balance of calcium within cells by acting as a calcium channel, and that the mutated forms of these genes lose this ability. Given the role that calcium signaling plays in cognitive function, it may be that this other role of presenilins is also important in the development of Alzheimer’s. If so, drugs that restore normal calcium levels might be useful for treating Alzheimer's disease.

Tu, H. et al. 2006. Presenilin Forms ER Ca2+ Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations. Cell, 126, 981–993.

http://www.eurekalert.org/pub_releases/2006-09/cp-ssa090106.php

New genetic cause of Alzheimer's disease

Amyloid protein originates when it is cut by enzymes from a larger precursor protein. In very rare cases, mutations appear in the amyloid precursor protein (APP), causing it to change shape and be cut differently. The amyloid protein that is formed now has different characteristics, causing it to begin to stick together and precipitate as amyloid plaques. A genetic study of Alzheimer's patients younger than 70 has found genetic variations in the promoter that increases the gene expression and thus the formation of the amyloid precursor protein. The higher the expression (up to 150% as in Down syndrome), the younger the patient (starting between 50 and 60 years of age). Thus, the amount of amyloid precursor protein is a genetic risk factor for Alzheimer's disease.

Theuns, J. et al. 2006. Promoter Mutations That Increase Amyloid Precursor-Protein Expression Are Associated with Alzheimer Disease. American Journal of Human Genetics, 78, 936-946.

http://www.eurekalert.org/pub_releases/2006-04/vfii-rda041906.php

Alzheimer's has higher genetic risk than thought

In a study far larger than any undertaken before, results suggest the highest estimates of the genetic risk of developing Alzheimer’s are in fact correct. The study involved all participants in the Swedish Twin Registry aged 65 or older in 1998 (nearly 12,000 of them) and found 392 pairs with evidence of Alzheimer's in at least one twin. In the model that best fit the data, genetic influence accounted for 79% of Alzheimer's risk, with 95% probability of being within the range 67 to 88%. The other 21% of Alzheimer's risk was due to non- shared environmental causes. Risk from shared environments was statistically negligible. Genetic risk for Alzheimer's was the same for men and women after controlling for age. The study raises doubts about the widely held view that Alzheimer's has two forms: the "familial," with genetic roots, and the "sporadic," with environmental causes. This doesn’t mean, however, that environment is unimportant.

Gatz, M. et al. 2006. Role of Genes and Environments for Explaining Alzheimer Disease. Archives of General Psychiatry, 63, 168-174.

http://www.eurekalert.org/pub_releases/2006-02/uosc-aft020206.php

Key genetic risk for Alzheimer's linked to myelin breakdown

Myelin, the fatty insulation coating the brain's internal wiring, builds up in childhood, and breaks down as we age. Myelin is critical for speedy communication between neurons. A new study supports a growing body of evidence that myelin breakdown is a key contributor to the onset of Alzheimer disease later in life. Moreover, it has also revealed that the severity and rate of myelin breakdown in healthy older individuals is associated with ApoE status. Thus both age, the most important risk factor for Alzheimer disease, and ApoE status, the second-most important risk factor, seem to act through the process of myelin breakdown.

Bartzokis, G., Lu, P.H., Geschwind, D.H., Edwards, N., Mintz, J. & Cummings, J.L. 2006. Apolipoprotein E Genotype and Age-Related Myelin Breakdown in Healthy Individuals: Implications for Cognitive Decline and Dementia. Archives of General Psychiatry, 63, 63-72.

http://www.eurekalert.org/pub_releases/2006-01/uoc--isl122805.php

Inactivation of Alzheimer's genes in mice causes dementia and brain degeneration

Mutations in two related genes known as presenilins are the major cause of early onset, inherited forms of Alzheimer's disease, but how these mutations cause the disease has not been clear. Since presenilins are involved in the production of amyloid peptides (the major components of amyloid plaques), it was thought that such mutations might cause Alzheimer’s by increasing brain levels of amyloid peptides. Accordingly, much effort has gone into identifying compounds that could block presenilin function. Now, however, genetic engineering in mice has revealed that deletion of these genes causes memory loss and gradual death of nerve cells in the mouse brain, demonstrating that the protein products of these genes are essential for normal learning, memory and nerve cell survival.

Saura, C.A., Choi, S-Y., Beglopoulos, V., Malkani, S., Zhang, D., Shankaranarayana Rao, B.S., Chattarji, S., Kelleher, R.J.III, Kandel, E.R., Duff, K., Kirkwood, A. & Shen, J. 2004. Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration. Neuron, 42 (1), 23-36.

http://www.eurekalert.org/pub_releases/2004-04/cp-ioa032904.php

Genes influence memory in families with Alzheimer's disease

A study of 1,036 people from 266 families, most of whom had more than one person living with Alzheimer's in the extended family, found that about half of the variation in memory performance among individuals was due to genetics. The influence of genetics was not as strong in the areas of attention, abstract reasoning, language and visual-spatial ability. The genetic influence seemed to have little to do with the gene apolipoprotein E, known to increase the risk of developing Alzheimer's. It should be noted, however, that participants in the study had an average of only six years of education.

Lee, J.H., Flaquer, A., Stern, Y., Tycko, B. & Mayeux, R. 2004. Genetic influences on memory performance in familial Alzheimer disease. Neurology, 62, 414-421.

http://www.eurekalert.org/pub_releases/2004-02/aaon-gim020304.php

Genes identified for age of onset of Alzheimer's

Genes responsible for controlling the age of onset of Alzheimer's or Parkinson's diseases in those individuals genetically predisposed to developing these diseases have been identified. It appears that chromosome 10, already thought to contain a risk gene for Alzheimer's disease, could also contain an age at onset gene that affects both Alzheimer's and Parkinson's diseases.

Li, Y. et al. 2002. Age at Onset in Two Common Neurodegenerative Diseases Is Genetically Controlled. American Journal of Human Genetics, 70, 985-993.

http://www.eurekalert.org/pub_releases/2002-02/dumc-dri022502.php

Evidence that Alzheimer's protein switches on genes

Amyloid b-protein precursor (APP) is snipped apart by enzymes to produce three protein fragments. Two fragments remain outside the cell and one stays inside. When APP is produced in excessive quantities, one of the cleaved segments that remains outside the cell, called the amyloid b-peptides, clumps together to form amyloid plaques that kill brain cells and may lead to the development of Alzheimer’s disease. New research indicates that the short "tail" segment of APP that is trapped inside the cell might also contribute to Alzheimer’s disease, through a process called transcriptional activation - switching on genes within the cell. Researchers speculate that creation of amyloid plaque is a byproduct of a misregulation in normal APP processing.

[2866] Cao, X., & Südhof T. C.
(2001).  A Transcriptively Active Complex of APP with Fe65 and Histone Acetyltransferase Tip60.
Science. 293(5527), 115 - 120.

http://www.eurekalert.org/pub_releases/2001-07/aaft-eta070201.php

New genetic risk factor for susceptibility to Alzheimer's disease

In a decade-long research study following more than 300 first-degree relatives of 189 Alzheimer's patients, researchers at the University of Pittsburgh have identified a small area of chromosome 10 that, when combined with the previously identified APOE E4 gene, significantly increase a person's risk of developing the disease. This combination of genes produced a 16-fold increase in the risk of AD among first-degree relatives. By comparison, this effect is greater than the increased risk of lung cancer caused by smoking. These new results are supported by independent studies of AD patients and controls from Pittsburgh, Boston, and Bonn, Germany.

The study was reported in Molecular Psychiatry, 6 (4), pages 413-419.

http://www.eurekalert.org/pub_releases/2001-06/MP-Ngrf-1706101.php

Gene marker for late-onset Alzheimer's disease nearer discovery

Three independent studies have linked late-onset Alzheimer's disease to a locus on chromosome 10 that affects processing of the amyloid-beta protein, a peptide important in the formation of the characteristic amyloid plaques found in the brains of people with Alzheimer's disease. Researchers are optimistic the precise gene will be found in the next few years.
Before this, a particular form of the apolipoprotein E (APOE) gene on chromosome 19 has been the only widely recognized genetic risk factor in late onset Alzheimer’s disease. There is also some evidence of a risk factor gene on a region of chromosome 12.
So far, three genes have been found that are linked to the rare early-onset Alzheimer's (when symptoms appear before age 60).

The findings are reported in the Dec. 22 issue of Science.

http://www.eurekalert.org/pub_releases/2000-12/MCJ-Loc1-2112100.php

Older news items (pre-2010) brought over from the old website

Study links Alzheimer's disease to abnormal cell division

Neurons affected by Alzheimer’s and many other neurodegenerative diseases often start to divide before they die. A new mouse study shows that this abnormal cell division starts long before amyloid plaques or other markers of the disease appear, suggesting a new approach to therapy for Alzheimer's. The findings also shed new light on the theory that the accumulation of amyloid beta in the brain causes the neuron death in Alzheimer’s, indicating that micro-molecular aggregates (tiny clumps made up of several amyloid beta molecules) rather than amyloid plaques may trigger the disease.

Yang, Y., Varvel, N.H., Lamb, B.T. & Herrup, K. 2006. Ectopic cell cycle events link human Alzheimer's disease and APP transgenic mouse models. The Journal of Neuroscience, 26 (3), 775-784.

http://www.eurekalert.org/pub_releases/2006-01/nion-sla011206.php

Abnormal cell division possible precursor of Alzheimer's

A study of genetically engineered mice sheds more light on the causes of Alzheimer’s. The study looked at what the reasons for neuron death apart from neurofibrillary tangles; they found an abnormal type of cell division occurring in tau proteins that may activate a cascade of abnormal events.

Andorfer, C., Acker, C.M., Kress, Y., Hof, P.R., Duff, K. & Davies, P. 2005. Cell-Cycle Reentry and Cell Death in Transgenic Mice Expressing Nonmutant Human Tau Isoforms. Journal of Neuroscience, 25, 5446-5454.

http://www.eurekalert.org/pub_releases/2005-06/ani-asa062005.php

Nerve cell death in Alzheimer's is caused by a failed attempt at cell division

Researchers have uncovered a key piece of missing evidence in the proof that nerve cell death in Alzheimer's disease is caused by a failed attempt at cell division. They have found a significant number of brain cells in Alzheimer's patients with extra copies of chromosomes, showing attempts at cell division in cells that are not supposed to divide. This effort to divide may be the cause of the nerve degeneration and dementia in Alzheimer's disease. "It's almost as if Alzheimer's disease were a novel form of cancer." Cancer is characterized by uncontrolled cell division. In this study, scientists found uncontrolled cell division, arrested in the midst of the process, is the likely cause of the nerve cell destruction. It is speculated that the plaques which are a hallmark of Alzheimer's disease brain cells trigger an inflammatory response in the brain, and that this response brings with it proteins that trigger cell division. This finding may signal a new approach to the treatment of Alzheimer's, trying to prevent signals for the inflammatory response from reaching the cells or to prevent the cells from responding to the signals to divide.

Yang, Y., Geldmacher, D. S., & Herrup, K. (2001). DNA Replication Precedes Neuronal Cell Death in Alzheimer’s Disease. The Journal of Neuroscience, 21(8), 2661–2668. Retrieved from http://www.jneurosci.org/content/21/8/2661

http://www.eurekalert.org/pub_releases/2001-04/CWRU-Rlfc-1604101.php

Overproduction of the brain chemical galanin might contribute to cognitive decline

Overproduction of the brain chemical galanin during the early stages of Alzheimer’s may have an negative effect on the brain and contribute to the cognitive decline of patients, according to a study involving transgenic (mutated) mice. The study suggests the overproduction of galanin might be a response to the deterioration of brain cells ( people with Alzheimer's have twice as much galanin in certain areas of the brain as peers who die of something else). While initially galanin might be beneficial, as the disease progresses, the overexpression of galanin may become its own problem, contributing to cognitive decline. It seems that the memory loss that occurs with Alzheimer's may be caused by the combination of cell death and excess galanin. It may be that a drug that blocks galanin would slow or reverse the mental damage caused by the disease.

Steiner, R. A., Hohmann, J. G., Holmes, A., Wrenn, C. C., Cadd, G., Juréus, A., … Crawley, J. N. (2001). Galanin transgenic mice display cognitive and neurochemical deficits characteristic of Alzheimer’s disease. Proceedings of the National Academy of Sciences, 98(7), 4184–4189. doi:10.1073/pnas.061445598 .

http://www.eurekalert.org/pub_releases/2001-03/RPSL-Oobc-1803101.php